Abstract
AbstractLateral root (LR) organogenesis is regulated by cellular flux of auxin within pericycle cells, which depends on the membrane distribution and polar localization of auxin carrier proteins. The correct distribution of auxin carrier proteins relies on the intracellular trafficking of these proteins aided by filamentous actin as a track. However, the precise role of actin in lateral root development is still elusive. Here, using vegetative class actin isovariant mutants, we revealed that loss of actin isovariant ACT8 led to an increase in lateral root formation. The distribution of auxin within pericycle cells was altered inact8mutant, primarily due to the altered distribution of AUX1 and PIN7. Interestingly, incorporation ofact2mutant inact8background (act2act8) effectively nullified the LR phenotype observed inact8mutant, indicating that ACT2 plays an important role in LR development. To explore further, we investigated the possibility that theact8mutant’s LR phenotype and cellular auxin distribution resulted from ACT2 overexpression. Consistent with the idea, enhanced lateral root formation, altered AUX1, PIN7 expression and auxin distribution in pericycle cells were observed in ACT2 overexpression lines. Collectively, these results suggest that actin isovariant ACT2 but not ACT8 plays a pivotal role in regulating source to sink auxin distribution during lateral root organogenesis.
Publisher
Cold Spring Harbor Laboratory